Hepatitis C, innate immunity and alcohol: Friends or foes?

Research output: Contribution to journalReview article

15 Citations (Scopus)

Abstract

Hepatitis C and alcohol are the most widespread causes of liver disease worldwide. Approximately 80% of patients with a history of hepatitis C and alcohol abuse develop chronic liver injury. Alcohol consumption in hepatitis C virus (HCV)-infected patients exacerbates liver disease leading to rapid progression of fibrosis, cirrhosis and even hepatocellular carcinoma. Hepatocytes are the main sites of HCV-infection and ethanol metabolism, both of which generate oxidative stress. Oxidative stress levels affect HCV replication and innate immunity, resulting in a greater susceptibility for HCV-infection and virus spread in the alcoholic patients. In this review paper, we analyze the effects of ethanol metabolism and other factors on HCV replication. In addition, we illustrate the mechanisms of how HCV hijacks innate immunity and how ethanol exposure regulates this process. We also clarify the effects of HCV and ethanol metabolism on interferon signaling—a crucial point for activation of anti-viral genes to protect cells from virus—and the role that HCV- and ethanol-induced impairments play in adaptive immunity which is necessary for recognition of virally-infected hepatocytes. In conclusion, ethanol exposure potentiates the suppressive effects of HCV on innate immunity, which activates viral spread in the liver and finally, leads to impairments in adaptive immunity. The dysregulation of immune response results in impaired elimination of HCV-infected cells, viral persistence, progressive liver damage and establishment of chronic infection that worsens the outcomes of chronic hepatitis C in alcoholic patients.

Original languageEnglish (US)
Pages (from-to)76-94
Number of pages19
JournalBiomolecules
Volume5
Issue number1
DOIs
StatePublished - Jan 1 2015

Fingerprint

Hepatitis C
Viruses
Innate Immunity
Hepacivirus
Alcohols
Ethanol
Liver
Metabolism
Oxidative stress
Adaptive Immunity
Virus Diseases
Alcoholics
Virus Replication
Liver Diseases
Hepatocytes
Oxidative Stress
Fibrosis
Viral Genes
Chronic Hepatitis C
Alcohol Drinking

Keywords

  • Dendritic cells
  • Ethanol
  • HCV
  • HCV RNA
  • Hepatocytes
  • Innate immunity
  • Interferon signaling
  • Toll-like receptors

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

Cite this

Hepatitis C, innate immunity and alcohol : Friends or foes? / Osna, Natalia A; Ganesan, Murali; Kharbanda, Kusum.

In: Biomolecules, Vol. 5, No. 1, 01.01.2015, p. 76-94.

Research output: Contribution to journalReview article

@article{e28b791d222f4d86a82c082182cb3f70,
title = "Hepatitis C, innate immunity and alcohol: Friends or foes?",
abstract = "Hepatitis C and alcohol are the most widespread causes of liver disease worldwide. Approximately 80{\%} of patients with a history of hepatitis C and alcohol abuse develop chronic liver injury. Alcohol consumption in hepatitis C virus (HCV)-infected patients exacerbates liver disease leading to rapid progression of fibrosis, cirrhosis and even hepatocellular carcinoma. Hepatocytes are the main sites of HCV-infection and ethanol metabolism, both of which generate oxidative stress. Oxidative stress levels affect HCV replication and innate immunity, resulting in a greater susceptibility for HCV-infection and virus spread in the alcoholic patients. In this review paper, we analyze the effects of ethanol metabolism and other factors on HCV replication. In addition, we illustrate the mechanisms of how HCV hijacks innate immunity and how ethanol exposure regulates this process. We also clarify the effects of HCV and ethanol metabolism on interferon signaling—a crucial point for activation of anti-viral genes to protect cells from virus—and the role that HCV- and ethanol-induced impairments play in adaptive immunity which is necessary for recognition of virally-infected hepatocytes. In conclusion, ethanol exposure potentiates the suppressive effects of HCV on innate immunity, which activates viral spread in the liver and finally, leads to impairments in adaptive immunity. The dysregulation of immune response results in impaired elimination of HCV-infected cells, viral persistence, progressive liver damage and establishment of chronic infection that worsens the outcomes of chronic hepatitis C in alcoholic patients.",
keywords = "Dendritic cells, Ethanol, HCV, HCV RNA, Hepatocytes, Innate immunity, Interferon signaling, Toll-like receptors",
author = "Osna, {Natalia A} and Murali Ganesan and Kusum Kharbanda",
year = "2015",
month = "1",
day = "1",
doi = "10.3390/biom5010076",
language = "English (US)",
volume = "5",
pages = "76--94",
journal = "Biomolecules",
issn = "2218-273X",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "1",

}

TY - JOUR

T1 - Hepatitis C, innate immunity and alcohol

T2 - Friends or foes?

AU - Osna, Natalia A

AU - Ganesan, Murali

AU - Kharbanda, Kusum

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Hepatitis C and alcohol are the most widespread causes of liver disease worldwide. Approximately 80% of patients with a history of hepatitis C and alcohol abuse develop chronic liver injury. Alcohol consumption in hepatitis C virus (HCV)-infected patients exacerbates liver disease leading to rapid progression of fibrosis, cirrhosis and even hepatocellular carcinoma. Hepatocytes are the main sites of HCV-infection and ethanol metabolism, both of which generate oxidative stress. Oxidative stress levels affect HCV replication and innate immunity, resulting in a greater susceptibility for HCV-infection and virus spread in the alcoholic patients. In this review paper, we analyze the effects of ethanol metabolism and other factors on HCV replication. In addition, we illustrate the mechanisms of how HCV hijacks innate immunity and how ethanol exposure regulates this process. We also clarify the effects of HCV and ethanol metabolism on interferon signaling—a crucial point for activation of anti-viral genes to protect cells from virus—and the role that HCV- and ethanol-induced impairments play in adaptive immunity which is necessary for recognition of virally-infected hepatocytes. In conclusion, ethanol exposure potentiates the suppressive effects of HCV on innate immunity, which activates viral spread in the liver and finally, leads to impairments in adaptive immunity. The dysregulation of immune response results in impaired elimination of HCV-infected cells, viral persistence, progressive liver damage and establishment of chronic infection that worsens the outcomes of chronic hepatitis C in alcoholic patients.

AB - Hepatitis C and alcohol are the most widespread causes of liver disease worldwide. Approximately 80% of patients with a history of hepatitis C and alcohol abuse develop chronic liver injury. Alcohol consumption in hepatitis C virus (HCV)-infected patients exacerbates liver disease leading to rapid progression of fibrosis, cirrhosis and even hepatocellular carcinoma. Hepatocytes are the main sites of HCV-infection and ethanol metabolism, both of which generate oxidative stress. Oxidative stress levels affect HCV replication and innate immunity, resulting in a greater susceptibility for HCV-infection and virus spread in the alcoholic patients. In this review paper, we analyze the effects of ethanol metabolism and other factors on HCV replication. In addition, we illustrate the mechanisms of how HCV hijacks innate immunity and how ethanol exposure regulates this process. We also clarify the effects of HCV and ethanol metabolism on interferon signaling—a crucial point for activation of anti-viral genes to protect cells from virus—and the role that HCV- and ethanol-induced impairments play in adaptive immunity which is necessary for recognition of virally-infected hepatocytes. In conclusion, ethanol exposure potentiates the suppressive effects of HCV on innate immunity, which activates viral spread in the liver and finally, leads to impairments in adaptive immunity. The dysregulation of immune response results in impaired elimination of HCV-infected cells, viral persistence, progressive liver damage and establishment of chronic infection that worsens the outcomes of chronic hepatitis C in alcoholic patients.

KW - Dendritic cells

KW - Ethanol

KW - HCV

KW - HCV RNA

KW - Hepatocytes

KW - Innate immunity

KW - Interferon signaling

KW - Toll-like receptors

UR - http://www.scopus.com/inward/record.url?scp=84943173851&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84943173851&partnerID=8YFLogxK

U2 - 10.3390/biom5010076

DO - 10.3390/biom5010076

M3 - Review article

C2 - 25664450

AN - SCOPUS:84943173851

VL - 5

SP - 76

EP - 94

JO - Biomolecules

JF - Biomolecules

SN - 2218-273X

IS - 1

ER -